Bilateral Wallerian degeneration of the medial cerebellar peduncles after ponto-mesencephalic infarction
Introduction
Wallerian degeneration of the tractus pyramidalis after lesions of the motor cortex or the brainstem is well described [1], [2], [3], [4] and independently of the kind of lesion, specific magnetic resonance imaging (MRI) signal changes develop in the corticospinal tract during the following months [5]. After peripheral and central lesions Wallerian degeneration is described such as degeneration within the optic nerves after lateral geniculate body lesion [4] or olivary degeneration after intracranial haemorrhage or trauma [6], [7], [8], [9], [10], [11]. In Wallerian degeneration myelinated fibres show a loss of the cytoplasmic circumferential bands and longitudinal columns and their associated membrane pores [12]. Macrophage recruitment for myelin removal also takes place [13]. These changes of demyelination lead to signal increase in T2-weighted images (T2w), which is also measurable by diffusion weighted imaging (DWI) [14], [15], [16], [17].
Section snippets
Patients
Three patients with acute paramedian ponto-mesencephalic brainstem infarction and consequent degeneration of the medial cerebellar peduncle were included.
CT/MRI
Computer tomography (CT) scan without application of contrast medium was performed immediately after admission of the patient to hospital. Up to three MRI were performed: the first MRI (MR0) in the first day after onset of symptoms or admission of the patient to hospital (echo planar imaging (EPI) DWI: TR/TE=4000/103 ms, with separately
General characteristics
There were three patients one men and two women (age 73, 62, 59 years) with acute ponto-mesencephalic paramedian brain stem infarctions. All three patients had initial symptoms of gait ataxia, dysarthria and contralateral hemiparesis with good improvement during the following 4–5 months. At the follow up only mild gait disturbance and slight hemiparesis was found.
MRI
In the acute phase all three patients had large paramedian ponto-mesencephalic stroke lesions covering the crossing area of the
Discussion
We describe three patients with first time acute brain stem stroke and corresponding large unilateral paramedian ponto-mesencephalic ischemic brain stem lesions. The majority of brain stem infarctions do not cross the midline [18], [19], [20]. Only in few cases, especially in basilar artery thrombosis, bilateral brain stem infarctions may occur [19], [20], [21].
Brain stem infarctions, except those due to basilary thrombosis, have a good prognosis concerning the clinical outcome [22]. Wallerian
Conclusion
Large paramedian lesions which cover the crossing zone of the medial cerebellar peduncles can lead to a bilateral Wallerian degeneration of the PCTs.
References (32)
- et al.
MRI demonstration of Wallerian degeneration in various intracranial lesions and its clinical implications
J. Neurol. Sci.
(1997) - et al.
Olivocerebellar retrograde trans-synaptic degeneration from the lateral cerebellar hemisphere to the medial inferior olivary nucleus in an infant
Brain Dev.
(1994) - et al.
The role of complement in myelin phagocytosis during PNS Wallerian degeneration
J. Neurol. Sci.
(1991) - et al.
Differentiation of dys- and demyelination using diffusional anisotropy
Pediatr. Neurol.
(1997) - et al.
Differentiation between dysmyelination and demyelination using magnetic resonance diffusional anisotropy
Brain Res.
(1995) - et al.
Time course of lesion development in patients with acute brain stem infarction and correlation with NIHSS score
Eur. J. Radiol.
(2001) - et al.
Organization of the pontine nuclei
Neurosci. Res.
(1992) - et al.
Diffusion-weighted imaging in Wallerian degeneration
J. Neurol. Sci.
(2000) - et al.
Water diffusion changes in Wallerian degeneration and their dependence on white matter architecture
Neuroimage
(2001) - et al.
MR detection of secondary changes remote from ischemia: preliminary observations after occlusion of the middle cerebral artery in rats
Am. J. Neuroradiol.
(1997)
The temporal and spatial activation of microglia in fiber tracts undergoing anterograde and retrograde degeneration following spinal cord lesion
J. Neurotrauma
MR-pathologic comparisons of Wallerian degeneration in spinal cord injury
Am. J. Neuroradiol.
The effects of Wallerian degeneration of the optic radiations demonstrated by MRI
Neuroradiology
Hypertrophy of the inferior olivary nucleus in patients with progressive supranuclear palsy
Eur. Neurol.
Midbrain tremor and hypertrophic olivary degeneration after pontine hemorrhage
Mov. Disord.
Thalamo-olivary degeneration in a patient with laryngopharyngeal dystonia
J. Neurol. Neurosurg. Psychiatry
Cited by (22)
Imaging secondary neuronal degeneration
2022, RadiologiaClinical Application of Diffusion Tensor Imaging in Chiari Malformation Type I– Advances and Perspectives. A Systematic Review
2021, World NeurosurgeryCitation Excerpt :Although the literature is sparse and the current data are based on single cohort studies, the authors of all studies outlined earlier suggest a specific pathology of MCPs associated with the symptomatic CMI presentation. A clinical presentation including ataxia, vertigo, dysarthria, and nystagmus might be observed not only in patients with CMI but also in individuals affected by a paramedian pontine stroke resulting in pontine nuclei injury and Wallerian degeneration of MCP fibers.41-43 Changes in DTI parameters observed in the latter entity include a decrease of AD as well as an increase of MD in MCPs and thus correspond with the findings of Eshetu et al.10 and Abeshaus et al.,18 respectively.
Bilateral wallerian degeneration of the middle cerebellar peduncles secondary to pontine infarction: A case series
2018, Journal of the Neurological SciencesCitation Excerpt :In our patients, bilateral MCPs show hyperintense on T2- weighted and FLAIR images on follow-up, which are correlated to histologic and metabolic features of the third stage of WD. There is also case reports that increased signal intensities in the MCPs on DWI can persist for 4 months later after stroke [16]. In our study, a slightly restricted diffusion in the MCPs is revealed in two patients on follow-up (mean time: 3.5 months).